The overall goal of this project is to elucidate pathophysiology and molecular genetic basis for gouty diathesis (stone formation associated with gout). Aim 1, concerned with pathophysiology, will test the hypothesis that a defective ammonium production may be uncovered by controlling acid intake and imposing phosphate restriction, and that in the acquired form of gouty diathesis, an insulin resistance is responsible for undue urinary acidity and other biochemical features of gouty diathesis. Aim 2 is directed at identifying the molecular defect in the ""primary"" form of the syndrome.